Atopic Dermatitis (Eczema): Pathophysiology, Triggers, and Multimodal Management

Atopic dermatitis (AD) is a chronic, relapsing, pruritic inflammatory skin disease with impaired barrier function and immune dysregulation.

Etiology

• Genetic: FLG (filaggrin) mutations → defective epidermal barrier → allergen penetration, water loss.
• Immune: Th2 skewing (IL-4, IL-13, IL-31) → IgE elevation, eosinophilia; later Th1/Th17/Th22 in chronic lesions.
• Environmental Triggers: Irritants (soaps, wool), allergens (dust mite, pet dander, pollen, mold, foods), climate (dry/cold), stress, sweat, microbes (S. aureus colonization).

Clinical Features

Age-dependent distribution: infants (face, scalp, extensors); children (flexures); adults (hands, eyelids, flexures). Intense itch → scratch cycle → lichenification.

Stepped Management

1. Foundation: Daily lukewarm baths, immediate thick emollient application (ceramide-containing), trigger avoidance, humidifier, cotton clothing, short nails.
2. Mild Flares: Low-potency topical corticosteroids (TCS) or calcineurin inhibitors (tacrolimus, pimecrolimus) for face/folds.
3. Moderate-Severe Flares: Mid-high potency TCS (short course), wet wraps, phototherapy (narrowband UVB).
4. Refractory/Severe: Systemic agents: dupilumab (IL-4Rα blocker), JAK inhibitors (upadacitinib, abrocitinib), traditional immunosuppressants (cyclosporine, methotrexate, azathioprine, mycophenolate).
5. Adjuncts: Antihistamines (sedating for sleep), bleach baths (decolonization), antibiotics for infection, counseling for psychosocial impact.

AD is manageable; early, consistent care prevents progression and improves quality of life.